Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin

J Bone Miner Res 2016, 31: 1791–1802. doi: 10.1002/jbmr.2869 PubMed PMID: 27163932Watch Full Movie Online Streaming Online and Download

In the context of glucocorticoid excess, activation of Wnt/β-catenin signaling by Sost/sclerostin deficiency sustains bone integrity by opposing bone catabolism despite markedly reduced bone formation and increased apoptosis. This crosstalk between glucocorticoids and Wnt/β-catenin signaling could be exploited therapeutically to halt resorption and bone loss induced by glucocorticoids and to inhibit the exaggerated bone formation in diseases of unwanted hyperactivation of Wnt/β-catenin signaling.

Autor: Sato, A. Y., Cregor, M., Delgado-Calle, J., Condon, K. W., Allen, M. R., Peacock, M., Plotkin, L. I. and Bellido, T.
Patrocinadores de la web
Laboratorios Rubió
Grupo Italfármaco
Gedeon Richter
Kyowa Kirin